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Tumor metaboception: local PGE2 signals global decline
Ming-Zhu Jin1, Hao-Ran Dang2, Wei-Lin Jin2
1Department of Obstetrics and Gynecology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200017, PR China; Shanghai Key Laboratory of Gynecologic Oncology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200017, PR China.
Trends in Molecular Medicine
|August 13, 2026
Summary
Cancer cachexia involves local signals, not just circulating factors. Liver kinase B1 (Lkb1)-mutant lung tumors release prostaglandin E2, causing anorexia and wasting via vagal neurons.
Area of Science:
- Oncology
- Neuroscience
- Metabolism
Background:
- Cancer cachexia is a complex syndrome characterized by involuntary weight loss.
- Previous research suggested circulating factors mediate cachexia, but local mechanisms remain under investigation.
Purpose of the Study:
- To investigate the role of local signaling in cancer cachexia, specifically in liver kinase B1 (Lkb1)-mutant lung tumors.
- To identify the molecular mediators and neural pathways involved in Lkb1-mutant lung tumor-induced cachexia.
Main Methods:
- Utilized a mouse model of Lkb1-mutant lung tumors.
- Investigated the effects of prostaglandin E2 (PGE2) on vagal nerve activity and feeding behavior.
- Assessed the impact of fat intake on cachexia progression.
Main Results:
- Demonstrated that local prostaglandin E2 (PGE2) produced by Lkb1-mutant lung tumors directly activates vagal neurons.
- Showed that this activation drives anorexia and contributes to systemic wasting.
- Found that fat intake accelerates the wasting process in this model.
Conclusions:
- Local PGE2 signaling from Lkb1-mutant lung tumors is a key driver of cancer cachexia.
- Introduced the concept of 'metaboception' – neural sensing of local metabolic signals.
- Suggests that targeting local signaling pathways, like PGE2-vagal neuron interactions, may offer novel therapeutic strategies for cancer cachexia.
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